We expierenced two cases of intradural verteral artery dissecting aneurysms. The presenting symptom was subarachnoid hemorrhage in one case and ischemic symptom in the other. The preoperative angiographic finding typically showed fusiform dilatation and proximal and/or distal narrowing of the affected artery. In one case, the vertebral artery was clipped distal to the PICA and in the other case trapping was performed through the extreme lateral transcondylar approaches. This approach permits a control of the aneurysm through the direct view of whole length of the vertebral artery, lower cranial nerves and ventral brain stem. In order to obtain ample view and to save the lower cranial nerves and perforating vessels, jugular tubercle should be sufficiently drilled out. Postoperitive neurological outcomes were favorable except mild hoarseness for some period in trapping case.
Aneurysm ; Aneurysm, Dissecting* ; Arteries ; Brain Stem ; Cranial Nerves ; Dilatation ; Hoarseness ; Pica ; Subarachnoid Hemorrhage ; Vertebral Artery

The present study investigates the effect of temporary selective brain cooling(SBC) on ischemic brain damage and edema on permanent middle cerebral artery(MCA) occlusion in the rat. Eighteen adult male Sprague-Dawley rats weighing 300-400g were used under halothane anesthesia. The brain temperature was monitored in the left caudate nucleus through a burr hole in the middle of the left coronal suture. All animals underwent left MCA occlusion via subtemporal approach. During the surgery, the physiological variables including mean arterial blood pressure were monitored continuously. Three groups of animals were studied: group 1. Normothermic brain themperature control(n=6) ; group 2, brain cooling for 30min(n=6) ; and group 3, brain cooling for 60min(n=6). In all groups, rectal temperature was maintaind 36.5 degrees C~37 degrees C, and in groups 2 and 3, brain temperature was lowered to less than 34 degrees C by active cooling. 15 min following MCA occlusion. After the brain cooling treatment, anesthesia was discontinued, and the animals were returned to the cage. Twenty-four hours following MCA occlusion, the rats were sacrificed. The volume of ischemic damage and edema was obtained by frozen section technique. There were no significant differences in all physiological parameters between normothermic and hypothermic animals, except the brain temperature. Postischemic SBC for either 30 or 60min significantly reduced the volume of infarction in the cerebral hemisphrere by 14%(p<0.05) or by 27%(p<0.01) respectively and also attenuated neurologic deficits observed at 24 hour postocclusion. However the volume of ischemic brain edema was not significantly reduced and the ratio of volume of brain edema/infarction increased signficantly in groups 2(p<0.05) and 3(p<0.05) compared with group 1. The present study demonstrates that postischemic temporary BSC can attenuate hemispheric infarction in a permanent focal cerebral ichemia model in the rat. However, ischemic brain edema appears not to be attenuated at all. The mechanisms of hypothermic protection and its clinical application are discussed.
Adult ; Anesthesia ; Animals ; Arterial Pressure ; Brain Edema ; Brain* ; Caudate Nucleus ; Cerebral Infarction* ; Edema* ; Frozen Sections ; Halothane ; Humans ; Hypothermia ; Infarction ; Male ; Neurologic Manifestations ; Rats ; Rats, Sprague-Dawley ; Sutures